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Local Change in Urinary Bladder Contractility Following CNS Dopamine Denervation in the 6-OHDA Rat Model of Parkinson's Disease

Journal article
Authors Reinika Mitra
Patrik Aronsson
Michael Winder
Gunnar Tobin
Filip Bergquist
Thomas Carlsson
Published in Journal of Parkinsons Disease
Volume 5
Issue 2
Pages 301-311
ISSN 1877-7171
Publication year 2015
Published at Institute of Neuroscience and Physiology, Department of Pharmacology
Pages 301-311
Language en
Links dx.doi.org/10.3233/jpd-140509
Keywords Urinary bladder pathophysiology, detrusor muscle, parasympathetic nervous system, muscarinic, CYCLOPHOSPHAMIDE-INDUCED CYSTITIS, QUALITY-OF-LIFE, IN-VITRO, NONMOTOR, SYMPTOMS, CONSCIOUS RATS, TRACT SYMPTOMS, DYSFUNCTION, RECEPTOR, SUPERSENSITIVITY, METHACHOLINE, Neurosciences
Subject categories Neurosciences

Abstract

Background: Urinary problems, including urinary frequency, urgency, and nocturia are some of the non-motor symptoms that correlate most with poor quality of life in Parkinson's disease. However, the mechanism behind these symptoms is poorly understood, in particular regarding peripheral bladder pathophysiology following dopamine degeneration. Objective: In this study, we compared the contractile responsiveness of urinary bladder from the 6-OHDA unilateral rat model of Parkinson's disease with that of normal untreated animals. Methods: The contractility of the urinary detrusor muscle was evaluated in bladder strip preparations using electrical field stimulation, and muscarinic and purinoceptor stimulations in an vitro organ bath setup. Results: Our data show that the overall contractile response following electrical field stimulation was significantly higher (43% at maximum contraction by 20-40 Hz stimulation) in the 6-OHDA-lesioned rats as compared to control animals. This increase was associated with a significant increase in the cholinergic contractile response, where the muscarinic agonist methacholine produced a 44% (at 10(-4) Mconcentration) higher response in the 6-OHDA-treated rats as compared to controls with a significant left-shift of the dose response. This indicates an altered sensitivity of the muscarinic receptor system following the specific central 6-OHDA-induced dopamine depletion. In addition a 36% larger contraction of strips from the 6-OHDA animals was also observed with purinoceptor activation using the agonist ATP (5x10(-3) M) during atropine treatment. Conclusions: Our data shows that it is not only the central dopamine control of the micturition reflex that is altered in Parkinson's disease, but also the local contractile function of the urinary bladder. The current study draws attention to a mechanism of urinary dysfunction in Parkinson's disease that has previously not been described.

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